ArticleJCI insight2022
NK cells contribute to reovirus-induced IFN responses and loss of tolerance to dietary antigen.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Viruses and celiac disease: what do we know ?Clinical and experimental medicine · 2023Pooled it
- Beyond Bacteria: The Emerging Role of the Gut Virome and Mycobiome in Celiac Disease.Nutrients · 2026Review
- Cocoa Attenuates Gluten-induced Pathogenesis in a Preclinical Model of Celiac Disease.Molecular nutrition & food research · 2026Article
- m6A RNA methylation modulates antiviral response in celiac disease.Genes and immunity · 2026Article
- Innate immune dysregulation in celiac disease and refractory celiac disease: mechanisms, management and emerging therapies.Frontiers in immunology · 2026Review
- Endogenous retroelements promote tolerance to dietary antigens.bioRxiv : the preprint server for biology · 2025Article
- Strain-specific differences in reovirus infection of murine macrophages segregate with polymorphisms in viral outer-capsid protein σ3.Journal of virology · 2024Article
- Gut microbiome in the first 1000 days and risk for childhood food allergy.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2024Review
- The role of tryptophan metabolism and tolerogenic dendritic cells in maintaining immune tolerance: Insights into celiac disease pathogenesis.Immunity, inflammation and disease · 2024Review
- The Role of Viruses in the Pathogenesis of Immune-Mediated Gastro-Intestinal Diseases.International journal of molecular sciences · 2024Review
- Non-Host Factors Influencing Onset and Severity of Celiac Disease.Gastroenterology · 2024Review
- An overview of the role of Niemann-pick C1 (NPC1) in viral infections and inhibition of viral infections through NPC1 inhibitor.Cell communication and signaling : CCS · 2023Review
- Paired immunoglobulin-like receptor B is an entry receptor for mammalian orthoreovirus.Nature communications · 2023Article
- Reovirus infection of tumor cells reduces the expression of NKG2D ligands, leading to impaired NK-cell cytotoxicity and functionality.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Celiac disease is an immune-mediated intestinal disorder that results from loss of oral tolerance (LOT) to dietary gluten. Reovirus elicits inflammatory Th1 cells and suppresses Treg responses to dietary antigen in a strain-dependent manner. Strain type 1 Lang (T1L) breaks oral tolerance, while strain type 3 Dearing reassortant virus (T3D-RV) does not. We discovered that intestinal infection by T1L in mice leads to the recruitment and activation of NK cells in mesenteric lymph nodes (MLNs) in a type I IFN-dependent manner. Once activated following infection, NK cells produce type II IFN and contribute to IFN-stimulated gene expression in the MLNs, which in turn induces inflammatory DC and T cell responses. Immune depletion of NK cells impairs T1L-induced LOT to newly introduced food antigen. These studies indicate that NK cells modulate the response to dietary antigen in the presence of a viral infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.